Cortical bone osteopenia substantially contributes to elevated fracture risk associated with aging. Aged cortical bone is distinguished by an expanded endocortical surface and elevated cortical porosity. Both of these adaptations degrade the strength of the material and its ability to resist failure. With the exception of non-human primates, no current animal model of skeletal aging naturally demonstrates both of these morphologic features. The primary purpose of this preliminary study is to determine the extent to which a novel cost-effective, vertebrate model mimics this bone loss. In addition, our preliminary data suggest that physical stimuli (i.e., disuse) precipitates local vasoregulation (i.e., hyperemia) in the young adult skeleton. As aging degrades the ability of the cardiovascular system to respond to external stimuli, we have hypothesized that the hyperemia precipitated by disuse is diminished in the aged skeleton. Two specific aims are proposed in which we will: i) quantify age induced alterations in avian cortical bone at the cell, material, and morphologic levels, and 2) determine whether bone vasoregulation induced by disuse is altered in the aged animal. From these data we will assess the viability of the aged rooster as a model of skeletal aging. Further, we will generate unique data regarding how a physiologic process (i.e., local vasoregulation) induced by disuse (a condition common in the elderly) is altered in aged bone.